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246 Cards in this Set
- Front
- Back
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Poiseuilles Law:
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Q= [(P)(Π)(r)^4]/(8)(n)(L)
flow equals pressure time pi times radius^4 divided by 8 times viscosity times length |
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what happens to flow as radius dec's?
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as radius dec's, flow exponentially dec's
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What happens to flow if length dec's (if P is constant)?
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inc'd flow if length dec's
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What happens to flow if viscosity inc's?
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dec;d flow
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what changes blood viscosity?
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-polycytemia vera(too many RBC's/hct in 60s)
-severe dehydration |
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arteries:
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-very elastic (spring back once expanded)
-very muscular -"resistance" vessels -relatively compliant -alpha 1 adrenergic receptors |
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veins:
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-"capacitance" vessels
-contains 2/3 of our blood at any moment -very compliant (expand in volume with v. small changes in BP) -not very elastic -have alpha 1 adrenergic receptors |
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why does BP go up as we naturally age?
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Blood vessels lose elastin and collagen resulting in dec'd compliance. LV stroke volume is still high, but stiff vessels don't comply and pressure goes up.
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What is arteriosclerosis?
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hardening of arteries due to changes in elastin and collagen in arteriolar walls; not as severe as athero
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What are the determinants of arterial BP?
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Physiologic:
-HR, SV, CO, TPR Physical: -viscosity, circulatory fluid volume, arterial compliance |
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Which receive sympathetic tone and change with neuronal activity?
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physiological
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are physical determinants short or long term?
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long
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What factors determine mean arterial pressure?
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CO and TPR
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what determines pulse pressure (Psystolic - Pdiastolic)
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SV and arterial compliance
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what are sounds of korotkoff?
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sounds heard while taking the BP- systolic and diastolic
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Mean arterial pressure=
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Pd + (Ps-Pd)/3 = 93 mmHg
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TPR=
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(Pa - Pra)/ CO= 1.12 mmHg*sec*mL^-1 = 1 PRU
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what is normal flow (Q)?
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=CO= 5L/min
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What happens to TPR in HTN?
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inc's; can go to 4 PRU during strong vasoconstriction
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what happens to TPR during exercise?
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goes down b/c arterioles open due to CO2 production....CO inc's which inc's BP.
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pulmonary vasc. resistance =
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(Ppulm art - Pla)/ CO = 0.08 mmHg*sec*mL^-1
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NL HR=
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60-80
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NL SV=
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83 mL/stroke
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NL CO=
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5L/min
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EDV=
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120mL (200-250 during exercise)
-when either ventricle has received all the blood it'll receive before it pumps |
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ESV=
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EDV- SV= 120-83= 37mL
10-20mL during exercise |
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EJ (ejection fraction)=
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SV/EDV= 83/120= 70%
90% during exercise 10%or lower in CHF |
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CI (cardiac index) =
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CO/m^2 = 5L/1.7 = 3
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Preload=
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EDV
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Afterload =
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aortic BP; highest BP in the body
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is diastolic active or passive?
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70% passive
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What are catecholamines?
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autonomic mediators/neurotransmitters: epinephrine, NE, and dopamine
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Epi aka adrenaline is secreted by:
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adrenal medulla
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epi is secreted into:
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the blood, then has access to all tissues
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What causes epi release?
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inc'd sympathetic tone during fight or flight
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what does epi's effect depend on?
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1. the predominant adrenergic receptor in that tissue and 2. the specific effect caused by agonism of that recpetor in that tissue
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which receptors does epi act on?
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1. B1 in the heart, 2. B2 in the bronchioles, 3. B2 in skeletal muscle arterioles, 4. a1 in skin and GI
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how does epi effect b1's in the heart?
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inc'd HR and contractility
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how does it affect b2 in the bronchs?
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bronch dilation
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how does it effect b2 in skelt. muscl arterioles?
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vasodilation
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how does it affect a1 in skin/GI?
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vasoconstriction
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how much of all catecholamines released by adrenal medulla are epi?
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80%
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how much are NE?
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less than 20%
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where is most important place NE is released from?
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sympathetic nerve terminals
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NE is complelty controlled by:
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autonomic NS
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autonomic storm::
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when inc'd sympathetic tone goes everywhere in the body (not just adrenal med)
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the effec of NE in each tissue depends on:
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1. predominant adgrenergic receptor in that tissue and 2. the specific effect caused by agonism
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which receptors does NE effect?
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1. B1 in the heart, 2. B2 in the bronchs, 3. B2 in the kids, 4. a1 in skeletal musc arterioles, 5. a1 in skin, GI and kids, 6. a2 in vasomotor ctr.
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B1 in heart:
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inc'd HR/contractility
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B2 in bronchs:
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dilation
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B2 in kids:
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renin secretion
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a1 in skel muscle arts:
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vasoconstriction
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a1 in skin, GI and kids:
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vasoconstriction
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a2 in vasomotor ctr.:
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dec'd symp outflow from cord
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what causes blushing:
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dec'd symp activity to vessels of the head neck sholders and upper chest permits vasodilation
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blanching?
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incd symp tone causes vasoconstriction.
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which system controls this?
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limbic
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is there metabolic (CO2) control associated with blushing/blancing?
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no, almost exclusively sympathetic
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what does cold ambient temp do?
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inc'd symp. tone to cutaneous vessels causes vasoconstriction to conserve heat....reverse alsso true
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what does inc'd blood temp do?
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dec'd symp tone to cutaneous vessels causes vasodilation to dissipate heat...reverse also true
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what happens during exercise?
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inc'd sympath. tone to cutaneous vessels cause vasoconstriction to shunt blood away. as body temp inc's hypothalamous permits cutaneous vasodilation to dissipate heat
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what controls skeleltal muscl arterioles at rest
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myogenic and sympathetic control
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during exercise?
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autoregulation (metabolic) takes over....inc'd CO2 causes vasodilation
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regulation of brain vasculature:
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autoregulation (myogenic and CO2). sympathetic vasoconstrictors are sparse
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regulation of coronary vasculature:
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innervated by sympathetic fibers that release NE
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in situ, what controls coronary vasc?
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mainly autoregulatory (like skel muscles/brain vessels). if heart works harder, arterioles dilate to supply more blood
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is heart influenced by PNS, SNS or both
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both
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which is acceleratory
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SNS
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deceleratory?
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PNS
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does PNS affect blood vessels elsewhere
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no
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what is vasovagal syncope?
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sudden, transient loss of consciousness (fainting): limbic system tells vasomotor system to withdraw all sympathetic tone which decelerates the heart into bradycardia and permits massive reflex dilation of all vessels. dilated veins dec's venous return to RA so CO from LV drops greatly causing rapid cerebral ischemia and you pass out.
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how does stress affect heart?
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limbic system interprets stressor and tells vasomotor center to send inc'd symp activity down spinal cord which affects a1 receptors in skel muscl arterioles/veins causing vasoconstriction. this increases TPR while venous constriction moves stored blood to heart. the inc'd symp tone to heart's b1 recepotrs cause inc'd contractility. SO, inc'd CO and inc'd TPR all lead to HTN.
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Diastolic heart murmurs:
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PI, MS, and AI
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systolic heart murmurs:
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TR, PS, MR, and AS
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what is TR?
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backward flow thru tricuspid valve
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most common cause?
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enlargement of the RV and dilation of the tricuspid annulus from RV failure
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TR pitch?
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high pitched blowing murmum
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other causes of TR?
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rheumatic fever (untreated), phen phen diet
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what is PS?
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forward flow thru pulmonary valve
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most common cause?
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birth defect- usually dx'd in childhood
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sx of PS?
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assymptomatic until adulthood, may cause HF in children
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tx of ps?
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heart surgery, valvuloplasty (balloon-tipped catheter threaded into valve and inflates separating leaflets)
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pitch of PS?
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crescendo-decrescendo murmur-LOUD (esp on inspiration)
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What is PI?
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backward flow thru pulm. valve
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PI pitch?
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high pitched blowing if no pulmonary HTN. if pulm HTN, then low-pitched
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aka
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pulmonary valve regurgitation or pulmonary incompetence
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occurs as a result of
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pulmonary HTN; may be congenital (or from surgery)
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sn/sx
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few or none besides murmur heard
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what causes pulm HTN?
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chronic lung disease, lung blood clots, endocarditis
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dx:
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pitch and location of murmur (high pitch blowing murmur at left 2nd intercostal space), EKG to detect flow change, echoCG w/color dop (and ultrasound imaging)to detect regurg, cxr shows pulm artery prominence; sometimes angiocardiography or artery xray with dye
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tx:
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seldom severe enough to require tx; antibios before dental work; management of primary condition (ie manage pulm HTN)
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what is MI (regurg)?
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backward flow thru insufficient mitral valve
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What happens during MI?
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as LV pumps blood into aorta, some leaks back into LA, inc'ing volume/pressure there which inc's pulm pressure (may result in lung congestion)
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causes?
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rheumatic fever (rare), heart attacke, myxomatous degeneration
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what is myxomatous degeneration?
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a hereditary connective tissue disorder that causes jellylike deterioration of tissue
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What does rheumatic fever (RF) mostly affect?
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mitral valve (95% of the time) but can also affect aortic....tricuspid is rare
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sx:
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mild- none; severe- palpitation while lying on left side; coughing SOBOE, leg edema (due to hrt failure)
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other complications
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atrial fib, blood clots-emboli, stroke, heart failure
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MI pitch:
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high
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what is mitral stenosis:
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reduced forward flow thru mitral valve causing volume and pressure of blood in LA to increase and LA enlarges
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MS almost always results from_________
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rheumatic fever
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when this is the cause, what happens to mitral valve cusps
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they're fused together
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other causes?
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congenital; also myxoma and blood clots can produce same effects as stenosis
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complications of MS if severe?
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heart failure w/ fluid accum in lungs, a-fib
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sn/sx
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easy fatigue, SOB, SOB while lying (due to hrt failure); severe- pulm HTN, hypoxemia, mitral facies (flush cheeks), hemoptosis, snapping sounding murmur
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dx:
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ECG, CXR, echoCG (w/ ultrasound)
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MS pitch:
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low rumbling- snapping sound
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aortic stenosis:
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forward flow thru a stenotic aortic valve
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what usually results from AS
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LVH b/c vent has to work harder to pump thru narrowed valve opening into aorta. leads to heart failure
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who does it mostly affect
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OLDER PEOPLE-due to scarring and calcium accumulation (calcification) in valve cusps YOUNG PEOPLE-congenital defect causes abnormal valve to become stiff and narrow due to calcification
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other causes
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RF (usually accompanied by MS)
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sn/sx
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angina and fainting on exertion; fatigue, SOBOE (with heart failure), and pulse abnormalities
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in someone with AS, why would BP drop suddenly during exercise?
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b/c arteries in skel muscle dilate during exercise, but narrowed vavle opening prevents LV from pumping enough to compensate
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what are complications of AS
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infective endocarditis
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dx:
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ECG indicates heart wall thickened, echoCG= best for measuring wall thickness,and color dop echoCG for rates of blood flow thru narrowed valve; cardiac catheterization tells how narrow and will show coronary artery narrowing, if any
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AS pitch:
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medium pitched crescendo-decrescendo murmur, ejection click
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what is AI?
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backward flow thru insufficient aortic valve
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what happens with AI?
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blood leaks back from aorta into LV, inc'ing volume and pressure. this inc's work and LVH results leads to heart failure.
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causes
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SEVERE: weakening of valves fibrous tissue due to myxomatous degeneration, unknown factors which can weaken, aortic aneumysms, and aortic dissection, infective endocarditis, and injury; MILD: severe high BP, birth defect with only two cusps instead of 3; RF and syphilis
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sn/sx:
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mild: none, SEVERE: palpitations, SOBOE, dyspnea while lying, possible night angina; collapsing pulse, characteristic murmur, ECG-enlarged LV, echoCG, coronary angiography
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tx:
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treat heart failure with drugs (digoxin, diuretics, calcium blockers, ACE inhibitors, or hydralazine plus nitrate) surgery usually required unless severe, pacemaker
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which drugs dilate BVs
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calcium blockers, ACE inhibitors, hydralazine plus nitrate, angioII receptor blocker
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pitch of AI:
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decrescendo murmur (pitch??)
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Heart failure =
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inability of heart to pump enough blood except when Pra and Pla are inc'd and circulatory vol is inc'd
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how do kidneys cause heart failure?
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a failing heart can't pump enough blood. circulating volume dec's, including flow and pressure to the kids. kids instinctively reabsorb Na+, Cl-, and H2O and secrete renin which inc's BP. unhealthy heart must now deal with inc's pressure and flow demands.
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what is compensated heart failure?
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as the failing heart labors to pump more blood, heart/peripheral vasculature need help so sympathetic tone inc's. as failure continues, heart continues to re-compensate. will last as long as compensation is possible
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what is decompensated heart failure?
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when there's no more sympathetic tone available and/or the heart cant respond
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What causes heart failure?
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ANYTHING THAT DAMAGES MYOCARDIUM: myocarditis, infectious endocarditis, constrictive pericarditis, cardiomyopathy, CAD, HTN, valvular disease, MI, PE, alcohol, hyperthyroidism, pregnancy, sepsis, and beriberi (thyiamine deficiency)
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which of these cause "high output failure"
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hyperthyroidism, pregnanncy, sepsis, and beriberi
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what does heart failure do to CO and venous pressures?
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CO dec's (LV and RV), venous pressure inc's: pulmonary if LVF and systemic if RVF
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what does dec'd CO and inc'd venous pressure do?
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causes renal compensation and sympathetic compensation
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what happens when compensations are exhausted and there's no more cardiac reserve?
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results in decompensated heart failure
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sn of decompensated HF?
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inc'd dyspnea, fatigue, edema, etc.
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typical causes of LVF:
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aortic stenosis or regurg, CAD (small vessel or large), and HTN
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What does CAD (small vessel) do?
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no major infarts but diffuse myocardium death
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what does CAD in general do
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AMI of LV
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sn/sx of LVF
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fatigue, pulmonary edema/pleural effusion, cough pink/brown sputum, wheezing (cardiac asthma), rales, DOE, PND (paroxysmal nocturnal dysp), orthopnea
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what causes DOE with LVF
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inc'd pulmonary venous pressure, dec'd pulmonary compliance, and inc'd airway resistance
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what does CXR show?
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cardiomegaly, cephalization of flow (inc's vascularity of lung apices), interstitial edema, Kerley B lines, plueral effusion, pulmonary artery enlargement
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what are kerly b lines
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water in the interlobular septa
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what causes RVF
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tricuspid regurgitation, CAD/AMI of RV, PS, PI, or MS
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sn/sx of RVF
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TYPICAL: fatigue, DOE, JVD and HJR, hepatosplenomegaly, hepatic dysfunction (inc'd bilirubin/AST/ALT), ascites, pedal edema; MISCELLANEOUS: confusion, insomnia, anorexia, weight gain, nocturia, renal failure
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what renal sn's show up with RVF
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oliguria, inc'd BUN and creatinine, proteinuria
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what sn show up with heart exam?
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heave or lift palpable on chest, 3rd and/or 4th heart sounds
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Causes of high output failure:
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Peripartum Cardiomyopathy, Thyrotoxicosis, Thiamine (B1) deficiency (Beriberi)
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peripartum cardiomyopathy:
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dilation; LV fails b/c it's supplying two people instead of one
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Thyrotoxicosis:
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inc'd basal metabolic rate leads to peripheral vasodilation and inc'd VR which inc's CO and leads to failure; OR the high BMR and/or thyroid h'mones weaken heart muscle themselves
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Thiamine B1 deficiency (beriberi):
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def. causes sign peripheral vasodilation, causing inc'd VR x 2 and then RVF; peripheral edema and ascites also result; B1 defic itself weakens heart muscle
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what are compensatory effects of inc'd sympathetic tone in compensatory HF?
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venoconstriction, inc'd contractility and HR, arteriolar constriction, renin secretion, ADH secretion
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result of venoconstriction:
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inc'd VR which leads to inc'd preload
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result of arteriolar constriction:
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inc'd TPR which leads to inc'd afterload
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result of renin secretion:
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angio II aldosterone secretion which inc's TPR and circulatory volume
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result of ADH secretion:
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inc'd renal H2O reabsorpion leads to in'cd circulatory volume and inc'd TPR
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total end effects of inc'd sympathetic tone:
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increased preload, increased afterload, increased TPR, and increased circulatory volume
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Systolic failure=
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failing ventricle has inadequate contractility
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Diastolic failure=
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failing vent is too stiff and noncompliant to properly fill during diastole
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"forward failure"
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systolic
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"backward failure"
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diastolic failure
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characteristics of SF
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decreased contractility, usually dilated ventricle, ejection fraction <40%, inadequate CO leads to fatigue and weakness
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what causes ventricular dilation?
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spiraling increase in circulatory fluid volume
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ex of SF
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Dilated cardiomyopathy
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characteristics of DF
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dec'd compliance and dec'd filling of ventricle, usually NL heart size maybe slight hypertrophy, NL ejection fraction, inc'd diastolic filling pressure w/o incd EDV, inc'd pulmonic or systemic pressures
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example of DF
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hypertrophic obstructive cardiomyopathy and constrictive pericarditis
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how does heart failure from CAD cause both SF and DF?
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SF from dec'd contractility from chronic myocardial ischemia and DF from fibrosis of destroyed myocardium
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differential diagnosis of HF (what to rule out with sn/sx presented):
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obesity-hypoventilation syndrome, COPD, pulmonary fibrosis, pneumonia, pneumothorax, pulmonary embolism, renal failure
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Tx:
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diuretics, ACE inhibitors, ARBs, Vasodilators (alpha1 blocker or direct), beta1 blockers, Ca channel blockers, and digoxin
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which is initial therapy for pt's with pedal and/or pulmonary edema
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diuretics, usually given with ACE inhibitors
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action of ACE inhibitors:
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angiotensin converting enzyme inhibitor slow or prevent ventricular remodeling (ventricular dilation)in heart failure
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why might a pt. switch from ACE inhibitor to Angio II receptor blockers?
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if they start experiencing annoying dry cough
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alpha1 and beta1 blockers, along with nitrates are:
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vasodilators
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how are beta blockers good for both diastolic and systolic failure
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DIASTOLIC: b/c they relax the heart
SYSTOLIC: b/c they block sympathetic renal and vasc tone |
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When are calcium channel blockers good?
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for diastolic failure b/c they relax the heart (but not systolic)
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What effect does digoxin have?
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A positive inotropic agent that: 1. inc's contractile force and 2. inc's parasympathetic tone to heart
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inc'd parasympathetic tone =
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dec'd SA node rate and inc'd AV node delay
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when is digoxin good?
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in moderate to severe systolic failure but not as first line
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angina =
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intermittent chest pain due to myocardial ischemia from inadequate coronary blood flow
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how is angina similar to intermittent claudication?
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both involve inadequate arterial flow due to atherosclerosis, result when O2 demand exceeds O2 supply
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what would pasieulle's law tell us when radius of the artery dec's?
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that flow will decrease exponentially
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why is the pain intermittent
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b/c as long as vessel isn't infarcted, there's still flow. when demand for flow inc's, pain sets in but leaves after exertion.
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3 types of angina:
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stable, variant, unstable
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Stable:
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"typical" or "classical", coronary stenosis due to atherosclerotic plaque, exertion causes pain, and pain relieved by rest
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Variant:
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Prinzmetal angina, temporary stenosis caused by coronary vasospasm, occurs at rest/awakens at night, women <50
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Unstable:
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existing stenosis worsened by acute change in atherosclerotic plaque and adherant partial thrombosis, less exertion causes more pain over time, more frequent attacks
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most common cause of stable angina?
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"critical stenosis" where it's a fixed atherosclerotic stenosis of one or more coronary arteries
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sometimes c/b
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AS, AI, or myocardial hypertrophy (diminished left output)
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sn/sx of stable
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a substernal sensation lasting 3-20 minutes, getting worse with exertion and relieved by rest
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description of substernal sensation
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pressure, crushing, tightness, burning, squeezing, vague pain
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where might sensation begin
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back of neck , lower jaw or interscapular area
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where does it radiate
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left shoulder, upper arm, inner aspect of elbow, forearm, wrist, or 4th/5th finger
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what may lower threshold of pain
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after meals, excitement, cold exposure
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DDx for any anginal type chest pain
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dissecting aortic aneurysm, pulmonary embolism, pneumothorax, pneumonia, esophageal spasm, GERD, peptic ulcer, cholecystitis, chest wall pain (Tietze's syndrome), cervical or thoracic radiculopathy
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what may be diagnostic of angina
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relief of pain after nitrate is administered (except can also relieve esophageal spasm)
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sn of angina during an attack:
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inc'd BP (sometimes dec'd), apical systolic murmur from mitral regurg (from papiallary muscle ischemia)
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historical sns:
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diabetes, HTN, PAD, xanthelasma (eyelid lipids)
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labs to order:
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serum lipids (cardiac lipids), glucose (rule out diabetes), iron (rule out anemia)
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What does resting ECG show
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NL in 1/4 of pt's with angina, non-specific ST-T changes in others
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what does anginal ECG show?
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ST segment depression which resolves after angina
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what does coronary angiography show
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stenosis of LAD coronary and/or branches
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other tests to order?
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stress test ECG
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tx of acute attack:
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nitro sublingually
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nitrate action:
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ARTERIOLAR DILATION: decreases TPR and afterload VENOUS DILATION: dec'd venous return and preload BOTH DEC. VENTRICULAR WORK/O2 DEMAND. CORONARY ARTERIOLE DILATION: BETTER FLOW
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prophylaxis
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avoid stress/emotional triggers, treat existing HTN and high LDLs. DRUGS: long acting nitrates, beta-blockers (to decrease HR/contractility and tissue O2 demand), calcium channel blockers (to dec. HR/contract and dilate coronaries), antiplatelet agents (ASA to prevent coronary thrombosis), coronary revascularization procedures (CABG, percutaneous transluminal coronary angioplasty-PTCA)
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cause of variant (prinzmetal) angina:
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unknown; not exertion-triggered
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sn/sx
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same as stable; pt. awakens in early morning
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ECG shows
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ST segment elevation (diff than classic)
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coronary angiography shows:
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no fixed stenoses, but shows right coronary artery involvement (spasm)
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tx
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CCBs or nitrates: Cardizem (diltiazem) or Verelan (verapamil)
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cause of unstable angina (aka crescendo/preinfarction)
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acute plaque change with adherant thrombosis and partial vessel occlusion
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sn/sx
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chest pain/sensation of inc'ing freq and intensity upon less exertion; attacks last longer than stable
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ECG:
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ST segment depression during attack, sometimes ST seg elevation
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Tx
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hospitalize, bed rest, limit activity, O2 supplementation; antiplatelet meds (ASA) and anticoagulants (non fractioned heparin or LMWH)
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nitrates used?
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yes but less responsive
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cause of AMI/heart attack
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most often fixed coronary atherosclerotic plaque causing critical stenosis PLUS acute plaque changes and/or coronary artery thrombosis
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what are acute plaque changes
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fissuring, hemorrhage into plaque, plaque rupture w/ embolization of debris
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what accounts for most AMIs in previously assymptomatice people
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acute plaque changes
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how do acute changes cause coronary artery thrombosis?
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plaque fissuring or rupture exposes platelets to thrombogenic plaque lipids and subendothelial collage
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how do cor art thrombs cause infarct
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by completely occluding vessel
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partial occlusion:
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unstable angina
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after infarct, when does myocardial necrosis begin
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20-30 mins
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where is first area to necrose
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subendocardial region
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why
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b/c its deepestand most poorly perfused- most closely adjacent to blood in the ventricular chamber, and it suffers high intramural contraction pressure during ventricular systole
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when does necrosis reach full efect
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3-6 hours- it spreads to middle and external heart layers
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transmural infarct:
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when necrosis encompasses most/all ventricualr wall thickness
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subendocardial infarct:
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when necrosis is restricted to the inner 1/3 of myocardium
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what determines size of infarct?
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1. lumen size where thrombus is (large lumen=large infarct), 2. degree of collateral circulation (hypervascularity)
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hypervascularity is a result of
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long term aerobic exercise, better chance of surving AMI
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OCCLUSION: LAD artery (40-50%)
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TISSUE INFARCTED: anterior and apical left ventricle, anterior 2/3 of interventricular septum
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left circumflex artery(15-20%):
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lateral wall of left vent
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right coronary artery (30-40%):
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posterior left vent wall, posterior 2/3 of intervent. septum; possibly right vent, AV, and SA nodes
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sx
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abrupt crushing chest pain in morning at rest, building to max intensity over a few mins., weakness, anxiety, diaphoresis, lightheadedness/syncope, wheeze/cough/dyspnea, N/V
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sn
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bradycardia or tachy, hypo or hypertension, respiratory distress, basilar rales, wheezing/extensive rales, peripheral cyanosis and/or claminess (from low CO)
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what does extensive rales/wheezing suggest
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pulmonary edema
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heart signs:
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almost NL or really abnormal heart exam, displaced PMI, JVD, S4 (atrial gallop), S3 (ventricular gallop), murmur of mitral regurg., pericardial friction rub
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displaced PMI=
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dyskinetic infarcted vent wall
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what causes JVD
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right atrial HTN from RV infarct or inc LV filling pressure from LV infarct
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what does S4 =
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LV dec'd wall compliance
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what does S3 =
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worse LV dysfunction
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what does murmur of mitral regurg suggest
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papillary muscle dysfunction or rupture
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why do 20% of AMI pt's die within the first hour
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from AMI induced V-fib
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is pedal edema common to see during infarct
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no
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classic evolution of ECG changes:
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1. tall peaked T waves, 2. ST segment elevation (firehat sign), 3. Q wave development (sometimes), 4. T-wave inversion
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non-Q wave infarct=
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an incomplete occlusion or some spontaneous lysis of thrumbus (non transmural infarct)
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Q-wave infarct=
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complete occlusion and signif transmural infarct
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Most infarcts are subendocardial or transmural:
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predominantly subendocardial with some trans extension, even in absence of Q waves
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Blood tests:
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Cardiac enzymes measured: CK-MB inc's within first 6 hrs, Troponin T and Troponin I are most specific for myocardial necrosis
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Tx
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ASA immediately, O2 supplementation, Morphine, thrombolytic therapy (reduce morbid/mortal in 1-3 hrs; high benefit to Q-wave infarcts), post MI therapy (beta blockers and ACE inhibitors)
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